Autoantibodies and autoimmune disorders in SARS-CoV-2 infection: pathogenicity and immune regulation

Darmarajan, Thiviya; Paudel, Keshav Raj; Candasamy, Mayuren; Chellian, Jestin; Madheswaran, Thiagarajan; Sakthivel, Lakshmana Prabu; Goh, Bey Hing; Gupta, Piyush Kumar; Jha, Niraj Kumar; Devkota, Hari Prasad; Gupta, Gaurav; Gulati, Monica; Singh, Sachin Kumar; Hansbro, Philip M.; Oliver, Brian G.; Dua, Kamal; Chellappan, Dinesh Kumar

doi:10.1007/s11356-022-20984-7

Cited by 13 publications

(19 citation statements)

References 140 publications

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“…Clinical and laboratory biomarkers have played a crucial role in assessing infection progression, enabling improved clinical management, and facilitating tailored therapies based on individual patient conditions (63)(64)(65). Although the fatality and infection rate of SARS-CoV-2 has decreased compared to the beginning of the pandemic and previous years thanks to the efficiency of vaccines, strains, and variants that are capable of avoiding this therapeutic measure still continue to emerge, which raises doubts about whether future booster doses are necessary despite the appearance of large epidemiological outbreaks of cases, and highlights the need to establish continuous surveillance systems against this pathogen and others with pandemic potential (66,67). Currently, the most pressing concern lies in the aftermath of COVID-19, with common sequelae including pulmonary fibrosis, respiratory distress, pulmonary thromboembolism, damage to the epithelium, and embolisms.…”

Section: Discussionmentioning

confidence: 99%

“…L452R mutation increase the interaction between RBD, the ACE-2 receptor and infectivity (66). T478K and L452R mutation helps to stabilize the RBD-ACE-2 complex and increases the infectivity rate of the virus (67). P681R mutation has been associated with an increased transmissibility and viral load (67).…”

Section: Sars-cov-2 and Its Infection Cyclementioning

confidence: 99%

“…T478K and L452R mutation helps to stabilize the RBD-ACE-2 complex and increases the infectivity rate of the virus (67). P681R mutation has been associated with an increased transmissibility and viral load (67). (171)(172)(173)(174).…”

Section: Sars-cov-2 and Its Infection Cyclementioning

confidence: 99%

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New insights into the pathogenesis of SARS-CoV-2 during and after the COVID-19 pandemic

Carvajal,

García-Castillo,

Cuellar

et al. 2024

Front. Immunol.

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is responsible for the respiratory distress condition known as COVID-19. This disease broadly affects several physiological systems, including the gastrointestinal, renal, and central nervous (CNS) systems, significantly influencing the patient’s overall quality of life. Additionally, numerous risk factors have been suggested, including gender, body weight, age, metabolic status, renal health, preexisting cardiomyopathies, and inflammatory conditions. Despite advances in understanding the genome and pathophysiological ramifications of COVID-19, its precise origins remain elusive. SARS-CoV-2 interacts with a receptor-binding domain within angiotensin-converting enzyme 2 (ACE2). This receptor is expressed in various organs of different species, including humans, with different abundance. Although COVID-19 has multiorgan manifestations, the main pathologies occur in the lung, including pulmonary fibrosis, respiratory failure, pulmonary embolism, and secondary bacterial pneumonia. In the post-COVID-19 period, different sequelae may occur, which may have various causes, including the direct action of the virus, alteration of the immune response, and metabolic alterations during infection, among others. Recognizing the serious adverse health effects associated with COVID-19, it becomes imperative to comprehensively elucidate and discuss the existing evidence surrounding this viral infection, including those related to the pathophysiological effects of the disease and the subsequent consequences. This review aims to contribute to a comprehensive understanding of the impact of COVID-19 and its long-term effects on human health.

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Section: Discussionmentioning

confidence: 99%

Section: Sars-cov-2 and Its Infection Cyclementioning

confidence: 99%

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New insights into the pathogenesis of SARS-CoV-2 during and after the COVID-19 pandemic

Carvajal,

García-Castillo,

Cuellar

et al. 2024

Front. Immunol.

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show abstract

“…Although our data suggest the antibody-mediated effects on neutrophil maturation and the suppression of neutrophil reactivity as a result of vaccination, it is worth mentioning that not all the antibodies have a protective effect in the inflammation. Autoantibodies, such as antinuclear antibodies (ANA) and antiplatelet autoantibodies (APA), are thought to be the causes of COVID-19 complications [ 37 , 38 ]. While APA are associated with thrombocytopenia, ANA can be responsible for the vasculitis in COVID-19 complications [ 39 , 40 ].…”

Section: Discussionmentioning

confidence: 99%

Short-Term Effect of SARS-CoV-2 Spike Protein Receptor-Binding Domain-Specific Antibody Induction on Neutrophil-Mediated Immune Response in Mice

Bolkhovitina

Vavilova

Bogorodskiy

et al. 2022

IJMS

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Vaccination protects against COVID-19 via the spike protein receptor-binding domain (RBD)-specific antibody formation, but it also affects the innate immunity. The effects of specific antibody induction on neutrophils that can cause severe respiratory inflammation are important, though not completely investigated. In the present study, using a mouse model mimicking SARS-CoV-2 virus particle inhalation, we investigated neutrophil phenotype and activity alterations in the presence of RBD-specific antibodies. Mice were immunized with RBD and a week after a strong antibody response establishment received 100 nm particles in the RBD solution. Control mice received injections of a phosphate buffer instead of RBD. We show that the application of 100 nm particles in the RBD solution elevates neutrophil recruitment to the blood and the airways of RBD-immunized mice rather than in control mice. Analysis of bone marrow cells of mice with induced RBD-specific antibodies revealed the increased population of CXCR2+CD101+ neutrophils. These neutrophils did not demonstrate an enhanced ability of neutrophil extracellular traps (NETs) formation compared to the neutrophils from control mice. Thus, the induction of RBD-specific antibodies stimulates the activation of mature neutrophils that react to RBD-coated particles without triggering excessive inflammation.

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“…Various autoantibodies, including antinuclear antibodies, anti–double-stranded DNA antibodies, anticitrullinated protein antibodies, antineutrophil cytoplasmic antibodies, and antiphospholipid antibodies, developed after COVID-19 13–15 . Furthermore, a recent study identified SARS-CoV-2–specific T cells in the synovium of patients with rheumatoid arthritis (RA) who had never experienced COVID-19 16 .…”

mentioning

confidence: 99%

Persistent Risk of Developing Autoimmune Diseases Associated With COVID-19

Inokuchi,

Shimamoto

2024

J Clin Rheumatol

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Objective This study aimed to investigate the risk of developing autoimmune diseases associated with coronavirus disease 2019 (COVID-19) in Japan, including long-term risks and risks specific to different variants of concern. Methods This observational study used an electronic medical record database in Japan. The COVID-19 group is composed of patients diagnosed with COVID-19, whereas the non–COVID-19 group had data sampled from the database. The outcomes of interest encompassed several autoimmune diseases, including rheumatoid arthritis, systemic sclerosis, and immunoglobulin G4–related disease, as well as a composite of these diseases (any autoimmune disease). We examined the relative risk of autoimmune diseases using standardized mortality ratio weighting and the Cox proportional hazards model. Subgroup analyses based on epidemic variants were performed. In addition, short- and long-term risks were investigated using piecewise constant hazard models. Results A total of 90,855 COVID-19 and 459,827 non–COVID-19 patients were included between January 16, 2020, and December 31, 2022. The relative risk of any autoimmune disease was 2.32 (95% confidence interval, 2.08–2.60). All the investigated outcomes showed a significant risk associated with COVID-19. Several autoimmune diseases exhibit a risk associated with COVID-19 in the short to long term, and the long-term risk is substantial for systemic sclerosis and immunoglobulin G4–related disease. The variant-specific risk varied across outcomes. Conclusions COVID-19 is associated with an increased risk of developing autoimmune diseases in the Japanese population, and this effect persists for a long time. This study provides insights into the association between viral infections and autoimmunity.

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Autoantibodies and autoimmune disorders in SARS-CoV-2 infection: pathogenicity and immune regulation

Cited by 13 publications

References 140 publications

New insights into the pathogenesis of SARS-CoV-2 during and after the COVID-19 pandemic

New insights into the pathogenesis of SARS-CoV-2 during and after the COVID-19 pandemic

Short-Term Effect of SARS-CoV-2 Spike Protein Receptor-Binding Domain-Specific Antibody Induction on Neutrophil-Mediated Immune Response in Mice

Persistent Risk of Developing Autoimmune Diseases Associated With COVID-19

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